American Association for Cancer Research

July 15 Cancer Research Highlights

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Selected Articles from the July 15, 2006 Issue

The articles referenced in this Highlights section will be available online in HTML and PDF formats to all interested users at no charge until the next issue of Cancer Research is published. Click on the article title to view the complete article.

View the Table of Contents for the July 15 issue of Cancer Research.


VHL Required for Primary Cilium Formation

Lutz and Burk
Page 6903
Mutations in the von Hippel-Lindau tumor suppressor gene, VHL, lead to hereditary and sporadic cancer syndromes including kidney polycystic disease and renal clear-cell carcinomas. Lutz and Burk examined the role of VHL in primary ciliogenesis, as loss or dysfunction of primary cilium is associated with essentially all forms of polycystic kidney disease. They showed a requirement for VHL in ciliogenesis, independent of VHL’s activity to degrade HIFα. This highlights VHL’s role in two distinct cellular pathways: differentiation/ciliogenesis and hypoxia-activated gene expression. The authors suggest a mechanism whereby disruption of both VHL functions is required for renal carcinogenesis.

 


Telomestatin Dissociates GFP-POT1 from Telomeres

Gomez et al.
Page 6908

CAN-07-15-06 Gomez 6908POT1 (protection of telomere 1) is a specific single-stranded telomere-binding protein involved in telomere capping and T-loop maintenance and is thought to regulate G-quadruplex conformation at the telomere. To explore its role in the mechanism of action of telomestatin, a potent G-quadruplex-interacting ligand with antitumoral properties, Gomez et al. examined binding of POT1 to a reconstituted telomeric overhang and the localization of GFP-POT1 to telomeric foci in human cells. The approach indicated that POT1 is rapidly and selectively removed from telomeres and confirms that telomestatin induces major modifications of the telomeric end structure, leading to the dysfunction of this essential telomere component.


Interactions between Cas and c-Src Induce Tamoxifen Resistance

Riggins et al.
Page 7007

Resistance to antiestrogens is a significant clinical problem in treating estrogen receptor–positive breast tumors. Riggins et al. investigated the mechanisms by which high expression of the scaffolding molecule Cas (also called BCAR1) confers resistance to tamoxifen. They found that Cas mediates tamoxifen resistance through its ability to bind to, and activate, the protein tyrosine kinase c-Src. Two substrates of c-Src, STAT5b and tyrosine 845 on the EGFR, were also found to be important for resistance. The identification of this Cas/c-Src/EGFR/STAT5 pathway as a mediator of tamoxifen resistance provides new avenues for therapeutic intervention geared toward reversing the resistance phenotype.

 


 

FUS-CHOP Fusion Model Suggests Origin of Myxoid Liposarcoma

Riggi et al.

Page 7016

CAN 07-15-06 Riggi 7016Mesenchymal progenitor cells (MPCs) are believed to constitute a common origin of at least a subset of sarcomas. Riggi et al. have recently observed that bone marrow-derived MPCs expressing the EWS-FLI-1 fusion protein form Ewing’s sarcoma-like tumors. Because MPCs colonize several tissues, including adipose tissue, they may also provide an origin of myxoid liposarcoma. In the present study, the authors show that MPC expressing the FUS-CHOP fusion protein form tumors with transcriptional and phenotypic features associated with human myxoid liposarcoma. These observations suggest that MPCs may constitute a candidate cell of origin of two distinct sarcomas and that, like EWS-FLI-1 in Ewing’s sarcoma, FUS-CHOP expression may initiate the pathogenesis of myxoid liposarcoma.


Signatures from 3D Mammary Acini Predict Breast Cancer Survival

Fournier et al.

Page 7095

Several groups have used transcriptional profiling of “training sets” of tumors to develop signatures predictive of outcome. Fournier et al. describe a novel unsupervised strategy to identify predictive signatures for breast cancer using 3D culture models of differentiating nonmalignant human mammary epithelial cells (HMECs). These cells proliferate for several days before forming growth-arrested, polarized mammary acini. A panel of genes was identified which distinguishes proliferative from quiescent HMECs in 3D culture, and breast tumors expressing the highest levels of this gene signature had the poorest outcome. This study underscores the value and potential clinical relevance of
3D culture models.